scholarly journals DNA vaccination with a gene encodingToxoplasma gondiiRhoptry Protein 17 induces partial protective immunity against lethal challenge in mice

Parasite ◽  
2016 ◽  
Vol 23 ◽  
pp. 4 ◽  
Author(s):  
Hai-Long Wang ◽  
Yu-Jing Wang ◽  
Yan-Jiang Pei ◽  
Ji-Zhong Bai ◽  
Li-Tian Yin ◽  
...  
1997 ◽  
Vol 186 (7) ◽  
pp. 1137-1147 ◽  
Author(s):  
Sanjay Gurunathan ◽  
David L. Sacks ◽  
Daniel R. Brown ◽  
Steven L. Reiner ◽  
Hughes Charest ◽  
...  

To determine whether DNA immunization could elicit protective immunity to Leishmania major in susceptible BALB/c mice, cDNA for the cloned Leishmania antigen LACK was inserted into a euykaryotic expression vector downstream to the cytomegalovirus promoter. Susceptible BALB/c mice were then vaccinated subcutaneously with LACK DNA and challenged with L. major promastigotes. We compared the protective efficacy of LACK DNA vaccination with that of recombinant LACK protein in the presence or absence of recombinant interleukin (rIL)-12 protein. Protection induced by LACK DNA was similar to that achieved by LACK protein and rIL-12, but superior to LACK protein without rIL-12. The immunity conferred by LACK DNA was durable insofar as mice challenged 5 wk after vaccination were still protected, and the infection was controlled for at least 20 wk after challenge. In addition, the ability of mice to control infection at sites distant to the site of vaccination suggests that systemic protection was achieved by LACK DNA vaccination. The control of disease progression and parasitic burden in mice vaccinated with LACK DNA was associated with enhancement of antigen-specific interferon-γ (IFN-γ) production. Moreover, both the enhancement of IFN-γ production and the protective immune response induced by LACK DNA vaccination was IL-12 dependent. Unexpectedly, depletion of CD8+ T cells at the time of vaccination or infection also abolished the protective response induced by LACK DNA vaccination, suggesting a role for CD8+ T cells in DNA vaccine induced protection to L. major. Thus, DNA immunization may offer an attractive alternative vaccination strategy against intracellular pathogens, as compared with conventional vaccination with antigens combined with adjuvants.


PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0153306 ◽  
Author(s):  
Dagoberto Sepúlveda ◽  
Niels Lorenzen

Vaccine ◽  
2004 ◽  
Vol 22 (13-14) ◽  
pp. 1717-1727 ◽  
Author(s):  
Volker Gerdts ◽  
Cemaine Tsang ◽  
Philip J. Griebel ◽  
Lorne A. Babiuk

2008 ◽  
Vol 83 (6) ◽  
pp. 2436-2445 ◽  
Author(s):  
Mario Lobigs ◽  
Maximilian Larena ◽  
Mohammed Alsharifi ◽  
Eva Lee ◽  
Megan Pavy

ABSTRACT The Japanese encephalitis virus (JEV) serocomplex, which also includes Murray Valley encephalitis virus (MVEV), is a group of antigenically closely related, mosquito-borne flaviviruses that are responsible for severe encephalitic disease in humans. While vaccines against the prominent members of this serocomplex are available or under development, it is unlikely that they will be produced specifically against those viruses which cause less-frequent disease, such as MVEV. Here we have evaluated the cross-protective values of an inactivated JEV vaccine (JE-VAX) and a live chimeric JEV vaccine (ChimeriVax-JE) against MVEV in two mouse models of flaviviral encephalitis. We show that (i) a three-dose vaccination schedule with JE-VAX provides cross-protective immunity, albeit only partial in the more severe challenge model; (ii) a single dose of ChimeriVax-JE gives complete protection in both challenge models; (iii) the cross-protective immunity elicited with ChimeriVax-JE is durable (≥5 months) and broad (also giving protection against West Nile virus); (iv) humoral and cellular immunities elicited with ChimeriVax-JE contribute to protection against lethal challenge with MVEV; (v) ChimeriVax-JE remains fully attenuated in immunodeficient mice lacking type I and type II interferon responses; and (vi) immunization with JE-VAX, but not ChimeriVax-JE, can prime heterologous infection enhancement in recipients of vaccination on a low-dose schedule, designed to mimic vaccine failure or waning of vaccine-induced immunity. Our results suggest that the live chimeric JEV vaccine will protect against other viruses belonging to the JEV serocomplex, consistent with the observation of cross-protection following live virus infections.


1998 ◽  
Vol 143 (1) ◽  
pp. 115-125 ◽  
Author(s):  
T.-Y. Ho ◽  
C.-Y. Hsiang ◽  
C.-H. Hsiang ◽  
T.-J. Chang

2000 ◽  
Vol 68 (1) ◽  
pp. 38-45 ◽  
Author(s):  
M. Vercammen ◽  
T. Scorza ◽  
K. Huygen ◽  
J. De Braekeleer ◽  
R. Diet ◽  
...  

ABSTRACT C57BL/6, C3H, and BALB/c mice were vaccinated with plasmids encoding Toxoplasma gondii antigens GRA1, GRA7, and ROP2, previously described as strong inducers of immunity. Seroconversion for the relevant antigen was obtained in the majority of the animals.T. gondii lysate stimulated specific T-cell proliferation and secretion of gamma interferon (IFN-γ) in spleen cell cultures from vaccinated BALB/c and C3H mice but not in those from control mice. Although not proliferating, stimulated splenocytes from DNA-vaccinated C57BL/6 mice also produced IFN-γ. No interleukin-4 was detected in the supernatants of lysate-stimulated splenocytes from DNA-vaccinated mice in any of the mouse strains evaluated. As in infected animals, a high ratio of specific immunoglobulin G2a (IgG2a) to IgG1 antibodies was found in DNA-vaccinated C3H mice, suggesting that a Th1-type response had been induced. For BALB/c mice, the isotype ratio of the antibody response to DNA vaccination was less polarized. The protective potential of DNA vaccination was demonstrated in C3H mice. C3H mice vaccinated with plasmid encoding GRA1, GRA7, or ROP2 were partially protected against a lethal oral challenge with cysts of two differentT. gondii strains: survival rates increased from 10% in controls to at least 70% after vaccination in one case and from 50% to at least 90% in the other. In vaccinated C3H mice challenged with a nonlethal T. gondii dose, the number of brain cysts was significantly lower than in controls. DNA vaccination did not protect BALB/c or C57BL/6 mice. Our results demonstrate for the first time in an animal model a partially protective effect of DNA vaccination against T. gondii.


2002 ◽  
Vol 70 (9) ◽  
pp. 4897-4901 ◽  
Author(s):  
Denis Martin ◽  
Stéphane Rioux ◽  
Edith Gagnon ◽  
Martine Boyer ◽  
Josée Hamel ◽  
...  

ABSTRACT The protective potential of antibodies directed against group B streptococcus (GBS) Sip surface protein was determined by using the mouse neonatal infection model. Rabbit Sip-specific antibodies administered passively to pregnant mice protected their pups against a GBS lethal challenge. In addition, active immunization with purified recombinant Sip protein of female CD-1 mice induced the production of specific antibodies that also confer protection to the newborn pups against GBS strains of serotypes Ia/c, Ib, II, III, and V. These data confirm that Sip-specific antibodies can cross the placenta and conferred protective immunity against GBS infections.


2016 ◽  
Vol 53 ◽  
pp. 66 ◽  
Author(s):  
N. Lorenzen ◽  
E. Lorenzen ◽  
J.S. Rasmussen ◽  
T.E. Kjaer ◽  
K. Einer-Jensen

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